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PubMed1998

Bradykinin may be involved in neuropeptide Y-induced diuresis, natriuresis, and calciuresis.

Neuropeptide Y (NPY) can cause diuresis, natriuresis, and calciuresis in rats independently of the pressure-natriuresis mechanism (A. Bischoff and M. C. Michel. Pflügers Arch. 435: 443-453, 1998). Because this is seen in systemic but not intrarenal NPY infusion, we have investigated the possible mediator of tubular NPY effects in anesthetized rats. In the present study, infusion of NPY (2 micrograms . kg-1 . min-1) enhanced renovascular resistance by approximately 8 mmHg . ml-1 . min and enhanced urine and sodium excretion by approximately 450 microliter/15 min and approximately 60-85 micromol/15 min, respectively. Acute renal denervation did not alter renovascular or tubular NPY effects, indicating that a neuronally released mediator is not involved. Treatment with the angiotensin II-receptor antagonist losartan prevented the decline of the renovascular response with time but did not modify tubular NPY effects. The bradykinin B2-receptor antagonist icatibant accelerated the decline of the renovascular NPY effects with time; concomitantly, it attenuated NPY-induced diuresis and natriuresis and abolished NPY-induced calciuresis. The converting-enzyme inhibitor ramiprilat prevented the decline of the renovascular response with time; concomitantly, it magnified the NPY-induced diuresis, natriuresis, and calciuresis. We conclude that bradykinin may be involved in NPY-induced diuresis, natriuresis, and, in particular, calciuresis.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1979

Fluid shifts during initial phase of immersion diuresis in man.

The object was to study fluid shifts in man during the 1st h of immersion diuresis. Control experiments were done on subjects lying down in air for 4 h with and without vasopressin. During immersion up to the neck, seven of nine subjects had significant diuresis and natriuresis. In the first 20 min of sitting in 33 degress C water, a hemodilution of 2% of blood volume was observed. As diuresis progressed, hemoconcentration began. When vasopressin was given just before immersion to prevent the diuresis, the hemodilution observed was greater and lasted longer. Thus the hematocrit fell by 1.7 U, plasma osmolality by 6.0 mosmol/kg, plasma proteins by 0.33 g/100 ml, and plasma sodium by 5.0 meq/l. We conclude that a hemodilution of about 4% of blood volume occurs during the early plasma of immersion and the degree of hyposmolality observed suggests that the fluid shifted was more hyposmotic than the interstitial fluid alone, possibly because some intracellular water may have shifted into the bloodstream during immersion.

Diuresis↗

PubMed2003

Relationship between natriuretic peptides and residual diuresis during continuous hemodiafiltration.

BACKGROUND: The reasons for the decrease or increase of urine output following the start of continuous venovenous hemodiafiltration (CVVHDF) have not yet been explained sufficiently. The renoprotective properties of natriuretic peptides were described. METHODS: The levels of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) were measured in 23 mechanically ventilated patients before and during the first 48 h of CVVHDF. Samples were drawn both from the ports proximal and distal to the filter. The results were compared between the group where daily diuresis (Vu) remained low or decreased and the group where diuresis increased to the level of 1.5 ml x kg(-1) x h(-1) or higher after 48 h of treatment. Left ventricular dysfunction (LVD) was defined as LV ejection fraction below 40%. A control group consisted of 10 patients exposed to abdominal surgery. RESULTS: The average AVdiff (%) of ANP and BNP on filter were insignificant. Patients with increasing diuresis (n = 12) had significantly lower levels of both ANP (p < 0.001) and BNP (p < 0.005) than the patients with decreasing diuresis (n = 11). Significant correlations were revealed for ANP and Vu (p < 0.01) and for BNP and Vu (p < 0.05). The levels of both peptides were grossly elevated in comparison to controls and were predictive of survival. The differences between cardiac and non-cardiac patients were significant both for ANP and for BNP. CONCLUSIONS: The elimination of ANP and BNP by the CVVHDF is negligible. The levels of natriuretic peptides are inversely related to Vu and predict survival. ANP and BNP levels correlate with left ventricular function even during acute renal failure and CVVHDF.

Acute Kidney Injury↗

PubMed2004

Low sodium excretion in SIADH patients with low diuresis.

UNLABELLED: It is well known that during low diuresis or low effective circulating volume, salt excretion is low. The aim of this study was to find out whether salt excretion, expressed as either urinary sodium concentration (UNa) or fractional sodium excretion (FENa), and the combined use of FENa and fractional urea excretion (FEurea) still differentiate between hyponatremic SIADH and hyponatremic salt depletion (SD) patients when diuresis is low. The relationships between UNa, FENa and diuresis, indirectly estimated by the urinary to plasma creatinine ratio (U/P creat), were studied in 42 hyponatremic SIADH patients, 21 hyponatremic SD patients and 66 normonatremic controls (CO) of similar age and sex ratio. There was no significant relationship between UNa and U/P creat either in SIADH or in SD or CO patients. FENa and U/P creat were inversely correlated, both in CO (r = -0.72; p < 0.001) and in SIADH (r = -0.68; p < 0.001). SIADH and SD patients can be fairly well differentiated from one another using FENa and U/P creat. Even with high U/P creat values, SIADH patients, despite a sharp decrease in their FENa values, presented still higher FENa values than SD patients did (mean FENa = 0.3 +/- 0.2% in SIADH and 0.1 +/- 0.04% in SD; p < 0.05). However, FENa values of SIADH patients with low diuresis (mean FENa = 0.3 +/- 0.2% for a mean U/P creat = 191 +/- 40) are indistinguishable from those of SD patients with normal urine volumes (mean FENa = 0.2 +/- 0.2% for a mean U/P creat = 92 +/- 30). The combined use of FENa and FEurea remains a reliable way to discriminate SD patients and SIADH patients, as far as the differential limit value for FENa is narrowed to a value of 0.15%, for hyponatremic patients with U/P creat >140. CONCLUSION: In SIADH, FENa values are lower than 0.5%, as soon as U/P creat exceeds a value of 180. In SD patients with U/P creat values exceeding 140, FENa is lower than 0.15% and FEurea lower than 45%.

Aged↗

PubMed2005

Effect of specific and non-specific inhibition of COX-2 on renal oxygenation before and after water diuresis.

BACKGROUND/AIMS: Water diuresis usually increases medullary oxygenation as a result of increased medullary synthesis of prostaglandins, but it is not clear whether this involves activation of cyclooxygenase-1 (COX-1) or cyclooxygenase-2 (COX-2). METHODS: The effects of celecoxib, a selective inhibitor of COX-2, and of ibuprofen, a non-specific inhibitor of COX-1 and COX-2, upon renal oxygenation during water diuresis were studied in a double-blind, prospective manner in 13 young women (age 24-34 years) using blood-oxygen level dependent magnetic resonance imaging. Celecoxib 200 mg b.i.d. for 4 days was compared with ibuprofen 80 mg b.i.d. for 4 days and with a placebo. RESULTS: There was no effect of either drug on urinary volume, urinary osmolal concentration, or creatinine clearance. Water diuresis alone elicited a significant increase in oxygenation in borderline areas between cortex and medulla, which was eliminated by celecoxib or ibuprofen. CONCLUSION: Renal medullary oxygenation is improved by water diuresis in normal young women in a way that is blocked by a selective inhibitor of COX-2 as well as non-selective cyclooxygenase inhibitors. Selective COX-2 may be expected to have significant effects on renal functions.

Adult↗

PubMed1983

The role of vasopressin suppression in phencyclidine-induced diuresis.

Phencyclidine (PCP; 10 mg/kg, s.c.) produced a marked diuresis which occurred without significant changes in solute excretion. This diuresis occurred predominantly within 2 h of PCP injection, and was blocked by pretreatment with vasopressin. The maximum diuresis corresponded temporally to a significant fall in plasma vasopressin and rise in mean arterial pressure. Thus, PCP-induced diuresis is due, at least in part, to suppression of plasma vasopressin. This suppression is probably related to the rise in blood pressure, though direct effects of PCP on the neurohypophysis cannot be excluded.

Animals↗

PubMed1984

Factors inducing post-obstructive diuresis in rats.

1 day after bilateral ureteral occlusion (BUO), the extracellular fluid (ECF) volume of rats was increased by 2.8 ml/100 g body weight above those values observed after either a sham operation or after 1 day of unilateral ureteral occlusion (UUO). The plasma urea concentration of BUO rats averaged about five times the values of either sham or UUO groups. The release of BUO of 1-day duration resulted in post-obstructive diuresis and natriuresis, whereas oliguria was observed after the release of UUO of 1-day duration. Contralateral nephrectomy of the normal kidney after the release of UUO 1-day duration (UUO-RN) resulted in an improvement of the damaged kidney functions, possibly due to an elevation of renal blood flow. Polyfructosan clearance of the UUO kidney was increased to a level significantly above the corresponding BUO value, 147 +/- 34 as compared to 101 +/- 8 microliters/min/100 g body weight. However, post-obstructive diuresis was not observed. When the ECF volume of UUO-RN rats was elevated, towards those values observed in BUO rats by saline infusion, the rate of urine formation was insignificantly elevated above the nontreatment group, even though the sodium excretion rate was increased about three times the values of both the UUO-RN and BUO groups. When the plasma urea concentration of the UUO-RN group was elevated towards the BUO value, moderate diuresis was observed. But when both the ECF volume and plasma urea concentration of UUO-RN rats were increased towards the level of the BUO rats, post-obstructive natriuresis and diuresis were evident.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1985

Ethanol-induced water diuresis is not prostaglandin dependent.

Previous studies have demonstrated an effect of alcohol on arachidonic acid metabolism. These studies were undertaken to determine if the water diuresis of alcohol is due to enhanced prostaglandin E2 (PGE2) production, a known antidiuretic hormone antagonist. 6 rabbits, weighing between 2.5 and 3.2 kg, were studied in standard metabolic cages during 4 periods: control, indomethacin administration, ethanol administration, and ethanol and indomethacin. 10 ml of 100% alcohol was added to their water in periods 3 and 4, and 5 mg/kg indomethacin was given during periods 2 and 4. We recorded urine output, urine osmolality, sodium excretion, potassium excretion, and PGE2 excretion. Urine flow rate significantly increased in periods 3 and 4 from 79 +/- 7 to 177 +/- 13 and 165 +/- 11 cm3/day, respectively, p less than 0.001 for both, compared to control. Indomethacin, therefore, did not prevent the water diuresis. Urinary PGE2 excretion was low (125 +/- 13 ng/day) with ethanol administration compared to control (897 +/- 71 ng/day, p less than 0.001). Levels were similar to those seen with the inhibitor indomethacin (105 +/- 22 ng/day, n.s.). These low levels with ethanol were observed at the same time of the significant free water diuresis. We conclude that the water diuresis produced by acute ethanol administration is not mediated by enhanced renal PGE2 production.

Animals↗

PubMed1983

Influence of diuresis on the degree of vesicoureteral reflux. An experimental investigation in rats.

The influence of bladder filling volume (BV), bladder pressure (BP) and diuresis (V) on the occurrence of vesicoureteral reflux (VUR) in Sprague-Dawley rats, where spontaneous VUR is common, has been investigated. The BV and BP at which VUR occurred during constant low diuresis (group I), high inconstant diuresis (group II) and moderately high, constant diuresis (group III), was measured. The abdomen was opened for visual observation of the VUR. The bladder was catheterized with a double-lumen metal catheter for infusion of a Lissamine green saline solution and to enable recording of BP. VUR occurred at significantly lower BV in group II than in group I and at significantly lower BV and BP in group I than in group III.

Animals↗

PubMed2000

A case of isolated ACTH deficiency who developed autoimmune-mediated hypothyroidism and impaired water diuresis during glucocorticoid replacement therapy.

A case of isolated ACTH deficiency who developed autoimmune-mediated hypothyroidism and still showed impaired water diuresis during glucocorticoid replacement therapy is reported. A 45-year-old woman was initially admitted for nausea, vomiting, and general malaise. Her serum sodium and plasma osmolality, ACTH and cortisol values were low, but her urine osmolality was high. Other pituitary hormone levels, thyroid hormone levels, and a computed tomogram of the pituitary gland were normal. The patient was treated with hydrocortisone and followed in the outpatient clinic; however, she was lost to follow up 18 months after admission. Three years later she presented with hypoglycemia and hyponatremia. Her serum or plasma ACTH, FT3, FT4, cortisol levels were low and her serum TSH level was high. Pituitary stimulation tests revealed a blunted response of ACTH to CRH and an exaggerated response of TSH to TRH. Plasma ADH was inappropriately high, and a water-loading test revealed impaired water diuresis and poor suppression of ADH. Although ADH was suppressed, impaired water diuresis was observed in the water loading test after hydrocortisone supplementation. Thyroxine supplementation completely normalized the water diuresis. Her outpatient clinic medical records revealed a gradual increase in TSH levels during follow up, indicating that she had developed hypothyroidism during glucocorticoid replacement therapy. The hyponatremia on the first admission was due to glucocorticoid deficiency, whereas the hyponatremia on the second admission was due to combined deficiencies of glucocorticoid and thyroid hormones.

Adrenal Insufficiency↗

PubMed2002

Effect of diuresis on P-wave duration and dispersion.

STUDY OBJECTIVE: To evaluate the effects of changing volume status on P-wave duration and dispersion in patients with decompensated heart failure. DESIGN: Prospective analysis. SETTING: Hospital cardiology unit. PATIENTS: Twenty-one patients with symptoms of decompensated heart failure who were treated with diuretics on admission. INTERVENTION: Twelve-lead electrocardiograms were obtained at baseline and after diuresis. Average, minimum, and maximum P-wave duration and P-wave dispersion (minimum minus maximum duration) were determined. MEASUREMENTS AND MAIN RESULTS: P-wave duration was measured manually in all 12 leads by using a 0.5-mm-scale precision ruler and magnifying lens. After 40+/-23 hours of diuresis, 3+/-1 L of fluid was removed. A significant correlation was found between average P-wave duration and amount of fluid removed (r = -0.59, p=0.015). Also, average and maximum P-wave duration were significantly decreased with diuresis (p=0.001 and 0.022, respectively). No other P-wave variables were significantly affected. CONCLUSIONS: Diuresis may attenuate electrophysiologic changes caused by fluid overload.

Aged↗

PubMed1991

Endothelin induces diuresis and natriuresis in the rat by acting on proximal tubular cells through a mechanism mediated by lipoxygenase products.

Besides being a potent renal vasoconstrictor, endothelin causes diuresis and natriuresis. At which site along the nephron and how endothelin alters water and sodium handling in the tubule remain to be clarified. It was found that endothelin (75 pmol) given as an i.v. infusion in vivo to rats caused diuresis and urinary sodium excretion to double but did not affect glomerular filtration rate and renal plasma flow. On raising the dose of endothelin to 150 pmol, a further increase in diuresis and natriuresis was found, whereas glomerular filtration rate fell 33% and renal plasma flow fell 36%; 300 pmol of endothelin reduced glomerular filtration rate by 73% and renal plasma flow by 77% but did not significantly affect diuresis and absolute sodium excretion. It did, however, increase fractional sodium excretion eightfold. Lithium clearance studies of changes in tubular handling of water and sodium indicated that infusion of 150 pmol of endothelin to rats caused a reduction in absolute (pre, 84.7 +/- 5.9; post, 47.9 +/- 6.1 microEq/min/100 g) and fractional (pre, 85.7 +/- 3.0; post, 64.7 +/- 6.4%) proximal reabsorption of sodium. Endothelin infusion (150 pmol) was not associated with any significant change in plasma atrial natriuretic peptide levels, which on average remained comparable to those in rats given the vehicle alone (49.7 +/- 8.4 versus 46.3 +/- 5.6 pg/mL). In the isolated perfused rat kidney preparation, exposure to 150 pmol of endothelin significantly increased fractional sodium excretion over preinjection values (pre, 2.2 +/- 0.2; post, 7.3 +/- 1.0%) despite a marked decrease in glomerular filtration rate and renal perfusate flow. Additional in vivo experiments showed that oral administration of the specific 5-lipoxygenase inhibitor L-651,392 to rats prevented the increase in urine flow rate (pre, 5.7 +/- 0.1; post, 6.6 +/- 0.8 microL/min), and in absolute (pre, 0.33 +/- 0.04; post, 0.37 +/- 0.05 microEq/min) and fractional (pre, 0.10 +/- 0.02; post, 0.11 +/- 0.03%) sodium excretion caused by bolus i.v. infusion of endothelin (150 pmol). Similarly, a specific leukotriene C4/D4 receptor antagonist, L-649,923, also prevented the diuretic and natriuretic effect of 150 pmol of endothelin i.v. infusion. These findings show that (1) endothelin has a diuretic and natriuretic effect that is independent of its action on renal hemodynamics; (2) this effect depends on a direct action on the proximal tubules; (3) atrial natriuretic peptide does not appear to be involved in this effect; and (4) the diuretic and natriuretic responses to endothelin are mediated by 5-lipoxygenase products.

Animals↗

PubMed1989

Effects of diabetes and diuresis on contraction and relaxation mechanisms in rat urinary bladder.

Experiments were designed to gain information on the mechanisms leading to diabetic urinary bladder dysfunction. Bladders from control rats, animals subjected to 4-5 wk streptozocin-induced diabetes, and rats subjected to equivalent diuresis produced by 5% sucrose feeding were studied with an in vitro whole-bladder preparation and neurochemical measurements. The diuretic group was used to distinguish alterations produced by metabolic effects on nerve and muscle from those induced by prolonged periods of excessive diuresis. Diuresis alone explains many of the diabetes-induced effects, including decreased norepinephrine levels, postsynaptic supersensitivity for sympathetic regulation of bladder storage, decreased responsiveness to parasympathetic regulation of emptying, and enhanced prostaglandin F2 alpha-induced contraction. Other diabetes-induced effects were not observed in the diuretic controls and are presumed to result from metabolic alterations associated with diabetes. These effects were decreases in norepinephrine uptake and in choline acetyltransferase activity, both markers of nerve terminal function. Thus, diuretic and metabolic factors appear to contribute to the early signs of parasympathetic and sympathetic neuropathy. In contrast, we found no evidence for loss of sensory nerve function in the diabetic bladder, at least at the organ level, because no diabetes- or diuresis-induced changes were observed in responsiveness to substance P or capsaicin.

Aminophylline↗

PubMed1982

Osmotic and osmotic-loop diuresis in brain surgery. Effects on plasma and CSF electrolytes and ion excretion.

In 22 patients to be operated on for brain tumors or cerebral aneurysms, the effect of osmotic diuresis was compared with that of osmotic-loop diuresis on plasma and cerebrospinal fluid (CSF) electrolytes, and water and ion excretion. Mannitol or mannitol plus furosemide were used to reduce brain bulk. After treatment with thiopental and hyperventilation, patients received randomly a rapid infusion of mannitol (1.4 gm/kg), or mannitol (1.4 gm/kg) plus furosemide (0.3 mg/kg). Brain shrinkage was considerably greater and more consistent with mannitol plus furosemide than with mannitol alone. However, hyponatremia, hypokalemia, hypochloremia, and hyperosmolality were also more marked (p less than 0.05) with mannitol plus furosemide than with mannitol. The rate of water and ion excretion was even more striking. At 30 minutes after absorption of mannitol alone, water excretion peaked at 17 ml/min, and gradually decreased to 3.8 ml/min 70 minutes later. With mannitol plus furosemide, during an identical time course, initial water excretion was 30 ml/min, followed by a further rise to 42 ml/min and then a decline to 17 ml/min. At peak diuresis after mannitol, Na+ and Cl- excretion average 0.57 and 0.62 mEq/min, respectively. This compares with mean values of 3.7 and 4.12 mEq/min for Na+ and Cl-, respectively, after mannitol plus furosemide. Although optimum brain shrinkage is achieved with osmotic-loop diuresis, the rapid electrolyte depletion (Na+ and Cl-) must be corrected to avoid altered sensorium during the patients' postoperative course.

Adult↗

PubMed1993

Contribution of plasma vasopressin concentration and blood pressure to norepinephrine-induced diuresis in conscious dogs.

Infusion of norepinephrine (NE) into humans and experimental animals induces diuresis by mechanisms that are not completely understood. Two series of experiments were performed to determine whether changes in plasma levels of vasopressin or changes in mean arterial pressure (MAP) are important-factors in NE-induced diuresis in conscious dogs. First, plasma vasopressin (PAVP) levels were measured in normal and cardiac-denervated conscious dogs during a 30-min intravenous infusion of NE (0.5 micrograms.kg-1.min-1). When NE was administered to normal dogs, urine flow increased from 0.3 +/- 0.1 to 0.9 +/- 0.4 ml/min. PAVP did not decrease, in spite of increases in mean arterial pressure (from 103 +/- 4 to 123 +/- 6 mm Hg) and left atrial pressure (from 5.2 +/- 0.9 to 8.6 +/- 1.4 mm Hg). The same dose of NE infused into cardiac-denervated dogs significantly increased urine flow (from 0.2 +/- 0.1 to 0.8 +/- 0.3 ml/min) and MAP (from 107 +/- 5 to 147 +/- 10 mm Hg), and decreased PAVP (from 1.8 +/- 0.3 pg/ml to 1.2 +/- 0.3 pg/ml). In the second series of experiments, NE was infused into cardiac-denervated dogs for 40 min. During the final 20 min of NE infusion, nitroprusside was infused to offset the pressor effect of NE by returning MAP to the initial control level. Urine flow increased during the first 20 min in which NE alone was given; however, when MAP was returned to the control level by nitroprusside infusion, urine flow also returned to the control level. PAVP increased from a control value of 3.6 +/- 0.6 to 18.9 +/- 3.8 pg/ml 15 min after the NP infusion had begun. We conclude that a decrease in PAVP is not required to elicit diuresis during NE infusion in normal conscious dogs and that the pressor effect of NE appears to play a major role in NE-induced diuresis.

Animals↗

PubMed2004

[Role of prostaglandin E2 in regulation of urine excretion in saluresis, water and osmotic diuresis in rat].

In the saluresis, water and osmotic diuresis were indicating an increase of prostaglandin E2 excretion and a correlation between this index and diuresis. Unselective blockade of cyclooxygenase by diclofenac-natrium leads to a decrease of diuresis in the observed types of urine-production in rats. Inhibition of inducible cyclooxygenase by celebrex didn't change the value of diuresis after water load or administration of osmotic agent, but decreased the diuretic effect of furosemide.

Animals↗

PubMed2006

Effects of long-term use of the heat-clearing, diuresis-promoting and collateral-mediating chinese drugs on changes of proteinuria in patients with chronic nephritis.

PURPOSE: To observe and evaluate the effects of long-term use of the heat-clearing, diuresis-promoting and collateral-mediating Chinese drugs on changes of proteinuria in patients with chronic nephritis, to analyze the influence of renal function, blood pressure, proteinuria and TCM syndrome types on therapeutic effects of the therapy, and to analyze the indications and effects of the heat-clearing, diuresis-promoting and collateral-mediating Chinese drugs when added with small dosage of Lei Gong Teng ([Chinese characters: see text] Radix et Rhizoma Tripterygii). METHOD: 43 cases of chronic nephritis were treated for one year with the heat-clearing, diuresis-promoting and collateral-mediating Chinese drugs. RESULT: A one-year treatment showed obvious reduction of proteinuria in patients with chronic nephritis. CONCLUSIONS: (1) The heat-clearing, diuresis-promoting and collateral-mediating Chinese drugs are effective for a long-term treatment of proteinuria in patients with chronic nephritis. (2) Additional use of Lei Gong Teng can help control proteinuria. (3) Damp-heat deeply accumulated in the kidney is one of the pathologic characteristics for chronic nephritis with the damp-heat syndrome.

Adult↗

PubMedDate not supplied

Water immersion induced alterations of plasma atrial natriuretic peptide (ANP), diuresis and natriuresis in kidney transplant patients.

UNLABELLED: The present article aimed to study the intactness of the physiological mechanism of ANP secretion in 64 kidney transplant patients treated with cyclosporine A + prednisone (CyA group--35 patients) or azathioprine + prednisone + promethasine respectively (Aza group or--29 patients). The control group comprised 15 healthy persons. ANP plasma levels were assessed before and 1 h and 2 h after neck out water immersion (WI). Higher basal ANP levels were found in patients of the CyA and Aza group than in normals (significantly higher in patients of the CyA group). WI induced an increase of plasma volume (PV) which was of comparable magnitude in all examined groups. It was accompanied by a significant increase of plasma ANP, diuresis and of natriuresis, which was significantly lower in transplanted patients than in normals. Only in healthy persons a significant positive correlation was found between the WI induced increase of plasma ANP and diuresis and natriuresis respectively. CONCLUSIONS: 1) kidney transplant patients are characterized by an intact, although reduced response of ANP secretion, diuresis and natriuresis to central hypervolaemia; 2) WI induced increase of diuresis and natriuresis does not seem to be only dependent upon ANP secretion in kidney transplant patients; 3) kind of immunosuppressive therapy seems to be of importance in the pathogenesis of altered ANP secretion in kidney transplant patients.

Adult↗